Table of Contents  
Year : 2012  |  Volume : 4  |  Issue : 1  |  Page : 7-10

Diabetes mellitus and oral health

Department of Oral and Maxillofacial Pathology, Ragas Dental College, Chennai, India

Date of Web Publication10-Sep-2012

Correspondence Address:
Ranganathan Kannan
Professor and Head, Department of Oral and Maxillofacial Pathology, Ragas Dental College, Uthandi, Chennai - 600096
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0975-8844.99874

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Diabetes mellitus is a group of metabolic disorders characterized by abnormal secretion and metabolic action of insulin. Hyperglycemia, the key feature of this endocrine disorder causes multisystem damage leading to untoward effects in various tissues collectively referred to as "Diabetic complications". Diabetes alters the oral health to a great extent. Indeed, periodontitis has been reported as the sixth complication of this disease. This article gives an overview of the oral effects of diabetes with an emphasis on periodontal disease and its relationship with cardiovascular disorders and pre-term birth. Dental considerations for management of these patients and recent advances in the dental field with respect to diabetes are also highlighted.

Keywords: Diabetes, oral, periodontal, dental

How to cite this article:
Radhika T, Kannan R. Diabetes mellitus and oral health. J Orofac Sci 2012;4:7-10

How to cite this URL:
Radhika T, Kannan R. Diabetes mellitus and oral health. J Orofac Sci [serial online] 2012 [cited 2022 Oct 3];4:7-10. Available from:

  Introduction Top

Diabetes mellitus (DM) is a multisystemic metabolic disorder characterized by abnormal carbohydrate, protein, and lipid metabolism. The cardinal biochemical feature of this disease is hyperglycemia, resulting from either a defect in insulin secretion from the pancreas, a change in insulin action, or both. Chronic hyperglycemia results in widespread multisystem damage, collectively referred to as, 'Diabetic complications,' which include retinopathy, neuropathy, nephropathy, macrovasular disease, and delayed wound healing. Diabetes is a looming health issue, constituting a huge global public health burden that is predicted to afflict300 million people globally by 2025, and at least 366 million people by 2030. [1]

Diabetes mellitus alters the cellular microenvironment in multiple organ systems, including the eyes, nerves, kidneys, and blood vessels. Oral cavity is not an exception. Diabetes has profound effects on oral tissues, particularly in individuals with poor glycemic control.

  Classification of Diabetes Top

The American Diabetes Association has proposed a classification scheme based on disease etiology, which includes two major forms - Type 1 and Type 2 diabetes. Type 1 disease includes type A (immune-mediated) and type B (idiopathic) DM. Type 2 includes the most common form, which combines insulin resistance and the insulin secretory defect. Other specific forms are diabetes secondary to autoimmune endocrinopathies, infection (congenital rubella, cytomegalovirus, coxsackie virus), genetic disease, and DM induced by drugs or pregnancy. [2]

  Pathophysiology of Diabetes Mellitus Top

Type 1 diabetes is caused by insulin deficiency, due to autoimmune destruction of pancreatic β-cells mediated by T cells and humoral mediators (Tumor necrosis factor, Interleukin-1, Nitric oxide). The pathophysiology of Type 2 diabetes is characterized by β-cell dysfunction, with relative insulin deficiency and peripheral insulin resistance.[3]

  Diagnostic Criteria for ­Diabetes Top

Fasting plasma glucose, two-hour plasma glucose during an Oral Glucose Tolerance test (OGTT), random plasma glucose levels, and glycosylated hemoglobin (HbA 1c ) levels are the diagnostic methods used for diabetes. The revised criteria suggest that diagnosis of DM can be made by any of the three methods, each requiring confirmation by repeat testing in the absence of unequivocal hyperglycemia [Table 1] (American Diabetes Association). [2]
Table 1: Criteria for the diagnosis of diabetes mellitus#

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  Diagnostic Methods for ­Diabetes Top

Blood glucose

Blood glucose test strips available in the market allow the patients to self-monitor their blood glucose levels, helping them to appropriately adjust their insulin dose on a day-to-day basis, and also encourage good compliance with dietary sugar intake. [4]

Glycosylated hemoglobin

The estimation of glycosylated hemoglobin (HbA1c) levels in the blood is an accurate method, and provides the measure of glycemic control over the past two to three months. Chronic hyperglycemia in diabetes causes slow, non-enzymatic, covalent attachment of glucose and other sugars (glycation) to hemoglobin. The rate of formation of this glycosylated hemoglobin is directly proportional to these ambient blood glucose concentrations. It is usually expressed as a percentage of the normal hemoglobin. HbA1c values of less than 6.5% indicate the absence of diabetes, while levels above 10% are indicative of poor glycemic control. The test plays a critical role in the management of a patient with diabetes. [2] Periodic evaluation of the HbA1c levels helps to overcome the disadvantage of inconsistency in the patient's records of home blood glucose monitoring.

Plasma fructosamine

Fructosamine assay is an index of glucose control and measures the levels of glycated serum protein (GSP). It is used in hemolytic anemias, where the HbA1c cannot be measured, and in diabetic pregnancy. A single measurement of GSP provides an index of the glycemic status over the preceding one to two weeks. [4]

Urine test

Testing for glucose in urine has been used as a method to monitor glycemic control for decades. The newer methods have almost replaced urine tests, as they permit much closer glycemic control. Negative urine tests fail to distinguish between normal and low blood glucose levels, which is a particular disadvantage, as the aim of treatment is to obtain the normal blood glucose level, avoiding hypoglycemia. Urine tests are routinely performed to monitor the levels of urinary proteins and ketones, to confirm the prior diagnosis of renal insufficiency in patients with DM. [4]

  Oral Manifestations of Diabetes Top

Diabetes and periodontitis

Periodontitis refers to inflammation of the tissues that surround and support the teeth. It is the most common chronic oral infection and often the major cause of tooth loss. Diabetes, particularly type 2 diabetes, is considered a risk factor for periodontitis. [5],[6],[7],[8],[9] Periodontitis has been reported as the sixth complication of diabetes. [10] The proposed mechanisms that explain the biological association between these diseases include, (1) microvascular alterations, (2) changes in components of gingival crevicular fluid, (3) changes in collagen metabolism, (4) altered host response, (5) altered subgingival flora, (6) genetic predisposition, and (7) non-enzymatic glycation. [11]

Not only does diabetes affect the periodontium, but evidence also suggests that periodontal infection may adversely affect the glycemic control of diabetes. [1],[7],[12] Periodontal therapy has shown reasonable improvement in glycemic control in diabetic patients with periodontitis. [7],1[3]

Diabetes and xerostomia

Xerostomia is a patient's subjective feeling of oral dryness. Both type 1 and type 2 diabetic patients have been reported to have xerostomia and salivary gland hypofunction. [14],[15] Factors that contribute to altered salivary function in diabetes include, hormonal, microvascular, and neuronal changes, caused by metabolic dysregulation, dehydration, or due to changes in the basement membrane of the salivary gland. [16] Persistent xerostomia compromises of the washing and protective function of saliva, thereby increasing the susceptibility to dental caries, oral mucosal soreness, and altered taste.

Diabetes and oral infections

Fungal infections of oral mucosal surfaces and removable prostheses are more common in adults with diabetes. Oral Candidiasis is the most common opportunistic fungal infection in diabetes, followed by zygomycosis and aspergillosis. Studies have shown increased oral Candida carriage in diabetics compared to non-diabetics. [17],[18],[19],[20] This could be attributed to increased salivary glucose levels, decreased salivary flow rate, or decreased candidacidal activity of the neutrophils. [17],[20],[21] Antifungal agents like nystatin are used commonly for the treatment of oral Candidiasis, but the most important aspect is to pursue the cause, which may even reveal the underlying, undiagnosed diabetes.

Diabetes and delayed wound healing

Changes in the collagen metabolism and host defense contribute to alterations in wound healing, in diabetic patients. Increased degradation of newly formed collagen, due to excessive production of collagenase and decreased solubility of the existing collagen, due to modification by the advanced glycation end products (AGEs), causes a shift in collagen turnover, thereby altering the healing response.

  Diabetes, Periodontitis, and Cardiovascular Disease Top

Sudden death due to cardiovascular events is common in patients with diabetes. Although numerous studies have reported separately on the association between periodontitis and diabetes, and periodontitis and coronary heart disease, the influence of periodontitis on the progression of cardiovascular disease in diabetes is less explored. Isolation of periodontopathic pathogens from atherosclerotic plaques have provided evidence for the association between periodontitis and coronary heart disease. [22] Upregulation of cytokines and other inflammatory mediators caused by the infection play a key role in the process. [11]

  Diabetes, Periodontitis, and Preterm Birth Top

Pregnant women with periodontal disease have been reported to be at a higher risk of preterm birth. [23],[24] Periodontal therapy for pregnant women with periodontitis has proved to be an efficient measure to reduce the incidence of preterm birth. [25] As diabetes is a potential risk factor for periodontitis, which in turn may cause preterm birth, timely and appropriate intervention for periodontitis in individuals with gestational diabetes proves to be a prudent measure to avoid preterm birth.

  Dental Care in Patients with Diabetes Top

Dental treatment procedures in patients with diabetes are similar to those provided for non-diabetic patients. However, few important considerations are essential to avoid complications like poor wound healing. Glycemic control of the patient should be monitored. Extensive dental surgical procedures should be avoided in patients with poor glycemic control, as endogenous production of epinephrine and cortisol increase during stressful situations. These hormones elevate the blood glucose levels and interfere with glycemic control. [26] Diabetic patients under insulin therapy will require an increase in insulin dosage in the presence of acute oral infection. [27]

Prophylactic antibiotic coverage prior to surgical therapy is preferred by few clinicians, if the diabetic patient's glycemic control is poor. Systemic antibiotics are usually considered in the presence of acute infection. Routine dental treatment in diabetic patients with good glycemic control does not require any antibiotic coverage. Certain medications used by the dentist may require adjustment of medical therapy for diabetes. Minor doses of systemic steroids given to diabetic patients with oral hypoglycemic agents can worsen the glycemic control. Such patients require short-term insulin therapy to maintain the blood glucose levels. [26]

  Recent Advances Top

Recent research has validated the use of salivary glucose levels as a non-invasive tool to monitor glycemic control in diabetes. [20],[28] An array of salivary biomarkers, including proteins and enzymes, have been discovered to non-invasively detect prediabetes / diabetes, which will facilitate timely interventions to prevent or delay progression to frank diabetes and its complications. [29],[30]

  Conclusion Top

Diabetes has profound effects on oral health. Increasing evidence of oral complications in diabetes warrants the inclusion of dental care as a part of primary health care in these patients. It is of paramount importance to provide good oral care for diabetic patients to combat complications, reduce the systemic inflammatory burden, prevent morbidity and mortality, and thereby, improve the quality of life of these individuals.

  Acknowledgment Top

Dr. N. Malathi MDS., Professor and Head, Department of Oral Pathology, Sri Ramachandra Dental College, Porur, Chennai, India

  References Top

1.Chen L, Wei B, Li J, Liu F, Xuan D, Xie B, et al. Association of periodontal parameters with metabolic level and systemic inflammatory markers in patients with type 2 diabetes. J Periodontol 2010; 81:364-71.  Back to cited text no. 1
2.American Diabetes Association. Diagnosis and Classification of Diabetes Mellitus. Diabetes Care 2011;34:S62-9.  Back to cited text no. 2
3.Kumar V, Abbas AK, Fausto N. Robbins and Cotran Pathologic Basis of Disease. 7th ed. 2005. p. 1189-205.  Back to cited text no. 3
4.Manfredi M, McCullough MJ, Vescovi P, Al-Kaarawi ZM, Porter SR. Update on diabetes mellitus and related oral diseases. Oral Dis 2004;10:187-200.  Back to cited text no. 4
5.Tsai C, Hayes C, Taylor GW. Glycemic control of type 2 diabetes and severe periodontal disease in the US adult population. Community Dent Oral Epidemiol 2002;30:182-92.  Back to cited text no. 5
6.Graves DT, Liu R, Alikhani M, Al-Mashat H, Trackman PC. Diabetes-enhanced inflammation and apoptosis: Impact on periodontal pathology. J Dent Res 2006;85:15-21.  Back to cited text no. 6
7.Taylor GW, Borgnakke WS. Periodontal disease: Associations with diabetes, glycemic control and complications. Oral Dis 2008;14:191-203.  Back to cited text no. 7
8.Lamster IB, Lalla E, Borgnakke, Taylor GW. The relationship between oral health and diabetes mellitus. J Am Dent Assoc 2008;139:19S-24.  Back to cited text no. 8
9.Chavarry NG, Vettore MV, Sansone C, Sheiham A. The relationship between diabetes mellitus and destructive periodontal disease: A meta-analysis. Oral Health Prev Dent 2009;7:107-27.  Back to cited text no. 9
10.Lowe GD. The relationship between infection, inflammation, and cardiovascular disease: An overview. Ann Periodontol 2001;6:1-8.  Back to cited text no. 10
11.Southerland JH, Taylor GW, Offenbacher S. Diabetes and Periodontal Infection: Making the Connection. Clin Diabetes 2005;23:171-8.  Back to cited text no. 11
12.Mealey SL, Fose LF. Diabetes mellitus and inflammatory periodontal disease. Current opinion in endocrinology. Curr Opin Endocrinol Diabetes Obes 2008;15:135-141.  Back to cited text no. 12
13.Simpson TC, Needleman I, Wild SH, Moles DR, Mills EJ. Treatment of periodontal disease for glycemic control in people with diabetes (Review). Cochrane Library 2010;5:CD004714.  Back to cited text no. 13
14.Moore PA, Guggenheimer J, Etzel KR, Weyant RJ, Orchard T. Type 1 diabetes mellitus, xerostomia and salivary flow rates. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2001;92:281-91.  Back to cited text no. 14
15.Chavez EM, Borell LN, Taylor GW, Ship JA. A longitudinal analysis of salivary flow in control subjects and older adults with type 2 diabetes. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2001;91:166-73.  Back to cited text no. 15
16.Chavez EM, Taylor GW, Borell LN, Ship JA. Salivary function and glycemic control in older persons with diabetes. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2000;89:305-11.  Back to cited text no. 16
17.Kadir T, Pisiriciler R, Akyuz S, Yarat A, Emekli N, Ipbuker A. Mycological and cytological examination of oral candidal carriage in diabetic patients and non-diabeticcontrol subjects: Analysis of local aetiologic and systemic factors. J Oral Rehab 2002;29:452-7.  Back to cited text no. 17
18.Belazi M, Velegraki A, Fleva A, Gidarakou I, Papanum L, Baka D, et al. Candidal overgrowth in diabetic patients: Potential predisposing factors. Mycoses 2005;48:192-6.   Back to cited text no. 18
19. Kumar BV, Padshetty NS, Bai KY, Rao MS. Prevalence of candida in the oral cavity of diabetic subjects. J Am Physicians India 2005;53:599-602.   Back to cited text no. 19
20. Sashikumar R, Kannan R. Salivary glucose levels and oral candida carriage in type II diabetics. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2010;109:706-11.  Back to cited text no. 20
21.Darwazeh AM, Macfarlane TW, McCuish A, Lamey PJ. Mixed salivary glucose levels and candidal carriage in patients with diabetes mellitus. J Oral Pathol Med 1991;20:280-3.  Back to cited text no. 21
22.Fiehn NE, Larsen T, Christiansen N, Holmstrip P, Schroeder TV. Identification of periodontal pathogens in atherosclerotic vessels. J Periodontol 2005;76:731-6.  Back to cited text no. 22
23.Khader YS, Ta'ani Q. Periodontal diseases and the risk of preterm birth and low birth weight: A meta-analysis. J Periodontol 2005;76:161-5.  Back to cited text no. 23
24.Marakoglu I, Gursoy UK, Marakoglu K, Cakmak H, Ataoglu T. Periodontitis as a risk factor for preterm low birth weight. Yonsei Med J 2008;49:200-3.  Back to cited text no. 24
25.Polyzos NP, Polyzos LP, Zavos A, Mauri D, Papanikolaou EG, Tzioras S, et al. Obstetric outcomes after treatment of periodontal disease during pregnancy: Systematic review and meta-analysis. BMJ 2010;341:c7017.  Back to cited text no. 25
26.Ship JA. Diabetes and oral health. J Am Dent Assoc 2003;134:4S-9S.  Back to cited text no. 26
27.Little JW, Falace DA, Miller CS, Rhodus NL. Diabetes. In: Little JW, editor. Dental management of the medically compromised patient. St. Louis: Mosby; 2002. p. 248-70.  Back to cited text no. 27
28.Amer S, Yousuf M, Siddiqiui PQ, Alam J. Salivary glucose concentrations in patients with diabetes mellitus - a minimally invasive technique for monitoring blood glucose levels. Pak J Pharm Sci 2001;14:33-7.  Back to cited text no. 28
29.Rao PA, Reddy AP, Lu X, Dasari S, Krishnaprasad A, Biggs E, et al. Proteomic identification of salivary biomarkers of Type-2 diabetes. J Proteome Res 2009;8:239-45.  Back to cited text no. 29
30.Ikekpeazu EJ, Neboh EE, Maduka IC, Anyanwu EG, Okenyi NS. Periodontal disease and type 2 diabetes: Effects on salivary enzyme activities. Int J Diabetes Dev Ctries 2011;31:9-13.  Back to cited text no. 30


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